Objective To investigate brachial artery endothelial function and carotid intima-media thickness (IMT) in patients with H-type hypertension.Methods One hundred and twenty patients with newly-diagnosed mild to moderate hypertension were enrolled in the study,including 58 cases with normal homocysteine (HCY) level (＜ 10 μmnol/L,non H-type group) and 62 cases with high HCY (≥10 μ moL/L,H-type group).Systolic pressure,diastolic pressure,blood lipid (TC,TG,LDL-C,HDL-C),fasting plasma glucose and two hours postprandial plasma glucose were measured in all patients.Brachial artery endothelial function and carotid IMT were determined with ultrasonography and compare between two groups.The factors related to brachial artery endothelium-dependent dilation (EDD) and carotid IMT were analyzed with multiple linear stepwise regression.Results Compared with non H-type group,the brachial artery EDD was reduced [(6.85 ± 0.77) ％ vs.(5.98 ± 0.85) ％,t =2.552,P =0.041] and carotid IMT was increased [(0.90±0.13)mm vs.(1.01 ±0.17)mm,t =2.426,P=0.048] in H-type group.The multiple linear stepwise regression analysis showed that EDD was negatively correlated to systolic pressure,diastolic pressure,fasting plasma glucose,two hours postprandial plasma glucose and HCY (r =-0.685,-0.654,-0.571,-0.627,-0.529,respectively,all P ＜ 0.05).IMT was positively related to systolic pressure,diastolic pressure,TC,TG,LDL-C and HCY (r =0.596,0.584,0.652,0.665,0.673,0.541,respectively,all P ＜ 0.05).Conclusion Patients with H-type hypertension are at a higher risk to arteriosclerosis than those with non H-type hypertension,which may be related to high HCY levels.

Objective To evaluate the effect of sevoflurane anesthesia on cognitive impairment in rats with traumatic brain injury. Methods One hundred and and twenty healthy male Wistar rats, aged 2-3 months, weighing 190-220 g, were assigned into 4 groups ( n=30 each) using a random number table method: control group ( group C) , traumatic brain injury group ( group T) , sevoflurane anesthesia group ( group S) , and traumatic brain injury plus sevoflurane anesthesia group ( group T+S) . A 40 g hammer was freely dropped onto the left parietal bone window from a height of 20 cm to establish the traumatic brain inju-ry model in T and T+S groups. Twelve days later, S and T+S groups inhaled 3％ sevoflurane for 3 h, and C and T groups inhaled pure oxygen for 3 h. On 1 day before anesthesia and 3 and 7 days after anesthesia, 10 rats in each group were randomly selected for performing Morris water maze test. Rats were sacrificed af-ter the end of Morris water maze test, and the hippocampal tissues were obtained for determination of the apoptosis rate of hippocampal neurons, cytoplasmic calcium concentration [Ca2+]i (by flow cytometry), expression of glucose-regulated protein 78 ( GRP78) and CCAAT∕enhancer-binding protein homologous pro-tein ( CHOP ) ( by immunohistochemistry ) , and expression of caspase-3 and caspase-12 ( by Western blot) . Results Compared with group C, the escape latency was significantly prolonged, the number of crossing platform was decreased, the apoptosis rate of hippocampal neurons and [ Ca2+] i were increased, and the expression of caspase-3, caspase-12, GRP78 and CHOP in hippocampal tissues was up-regulated in S, T and T+S groups ( P<0. 05) . Compared with T and S groups, the escape latency was significantly prolonged, the number of crossing platform was decreased, the apoptosis rate of hippocampal neurons and [ Ca2+] i were increased, and the expression of caspase-3, caspase-12, GRP78 and CHOP in hippocampal tissues was up-regulated in group T+S ( P<0. 05 ) . Conclusion Sevoflurane anesthesia can accentuate cognitive impairment in rats with traumatic brain injury, and the mechanism may be related to aggravating the degree of endoplasmic reticulum stress-induced calcium overload and increasing the apoptosis rate of hip-pocampal neurons.

Objective To evaluate the effect of laparotomy on cognitive function in rats with trau-matic brain injury and the relationship with calcium overload. Methods One hundred and fifty healthy male Wistar rats,aged 2~3 months,weighing 190~220 g,were assigned into 5 group ( n=30 each) using a ran-dom number table:blank group(group B),surgery group of blank rats(group BS),surgery group of sham rats (group SS),traumatic brain injury rats group( group T),surgery group of traumatic brain injury rats(group TS). TBI model was made in rats of group T and TS by Feeney method. Rats in group SS were only treated with cranial bone window without crainocerebral impact. Both group B and BS were normal rats. Then the rats in group BS,SS and TS group underwent laparotomy under sevoflurane anesthesia (the operation time was a-bout 3 hours) and the rats in group B and T inhaled pure oxygen for 3 hours after 20 days. One day before surgery,3 and 7 d after surgery,10 rats in each group were randomly selected for Morris water maze test. The hippocampus tissue of 10 rats were taken after the water maze test. The apoptosis rate and calcium concen-tration of hippocampal neurons were measured by flow cytometry,and the expression level of cleaved caspase-3 in hippocampal tissues was determined by Western blot. Results One day before surgery,compared with group B(the escape latency(9. 8±0. 8)s,the number of crossing platform (5. 8±0. 8),the apoptosis rate of hippocampal neurons ( 2. 5 ± 0. 9)%, calcium ion concentration ( 2. 3 ± 0. 2),the expression of cleaved caspase-3 (0. 22±0. 07) ),the escape latency of group T and group TS were prolonged (group T:(25. 5± 0. 7)s,P<0. 05;group TS:(25. 1±1. 1) s,P<0. 05),the number of crossing platform decreased (group T:(2. 7±0. 8),P<0. 05;group TS:(2. 8±0. 6),P<0. 05),the apoptosis rate of hippocampal neurons increased (group T:(5. 3±0. 6)%,P<0. 05;group TS:(5. 2±1. 0)%,P<0. 05),calcium ion concentration increased (group T:(3. 7±0. 4),P<0. 05;group TS:(3. 6±0. 5),P<0. 05) and the expression of cleaved caspase-3 increased (group T:(0. 45±0. 07),P<0. 05;group TS:(0. 44±0. 05),P<0. 05),the differences were statis-tically significant. Compared with the group SS,the escape latency ( 3 d after surgery:group SS:( 23. 8 ± 1. 3)s,group TS:(56. 4±2. 5)s,P<0. 05;7 d after surgery:group SS:(16. 6±1. 8)s,group TS:(38. 1±2. 1) s,P<0. 05)of the rats in group TS were prolonged,the number of crossing platform decreased (3 d after sur-gery:group SS:(2. 9±0. 6) ,group TS:(1. 1±1. 1) ,P<0. 05;7 d after surgery:group SS:( 4. 2± 1. 2) , group TS:(1. 7±1. 3),P<0. 05),the apoptosis rate of hippocampal neurons ( 3 d after surgery:group SS:(4. 8±0. 6)%,group TS:(14. 4± 0. 6)%,P<0. 05;7 d after surgery:group SS:(3. 8± 1. 1)%,group TS:(9. 6±1. 3)%,P<0. 05),calcium ion concentration ( 3 d after surgery:group SS:(3. 1± 0. 3),group TS:(6. 4±0. 5),P<0. 05;7 d after surgery:group SS:( 2. 6± 0. 3),group TS:( 4. 8± 0. 4),P<0. 05) ,the ex-pression of cleaved caspase-3 (3 d after surgery:group SS:( 0. 42± 0. 03),group TS:( 0. 88 ± 0. 08),P<0. 05;7 d after surgery:group SS:(0. 33±0. 05),group TS:(0. 63±0. 06),P<0. 05) in the hippocampus in-creased after surgery (P<0. 05). Compared with the T group,the escape latency (3 d after surgery:group T:( 18. 6±2. 0)s,group TS:(56. 4±2. 5)s,P<0. 05;7 d after surgery:group T:(13. 8±2. 6)s,group TS:(38. 1 ±2. 1)s,P<0. 05) of the rats in group TS were prolonged,the number of crossing platform (3 d after surger-y:group T:(3. 4±0. 5),group TS:(1. 1±1. 1),P<0. 05;7 d after surgery:group T:(4. 3±1. 2),group TS:(1. 7±1. 3),P<0. 05) decreased,the apoptosis rate of hippocampal neurons (3 d after surgery:group T:(4. 4±0. 7)%,group TS:( 14. 4 ± 0. 6)%,P<0. 05;7 d after surgery:( 3. 3 ± 1. 3)%,group TS:( 9. 6 ± 1. 3)%,P<0. 05),calcium ion concentration (3 d after surgery:group T:( 3. 4 ± 0. 4),group TS:( 6. 4 ± 0. 5),P<0. 05;7 d after surgery:group T:(3. 0±0. 3),group TS:(4. 8±0. 4),P<0. 05),the expression of cleaved caspase-3 (3 d after surgery:group T:(0. 40±0. 04),group TS:( 0. 88±0. 08),P<0. 05;7 d after surgery:(0. 35±0. 02),group TS:(0. 63±0. 06),P<0. 05) in the hippocampus increased after surgery(P<0. 05). Conclusion Laparotomy can aggravate the cognitive impairment of rats with traumatic brain injury and cause postoperative cognitive impairment,which may be related to the increased degree of calcium over-load and the increased rate of hippocampal neuron apoptosis.

The effectiveness of rhIL-11 on thrombocytopenia induced by carboplatin in rhesus monkeys was investigated. Thrombocytopenia was induced in monkeys by i.v. administration of carboplatin at a dose of 15 mg/kg(-1)/d(-1) for three consecutive days. rhIL-11 (50 or 100 micro g/kg(-1)/d(-1)) or Neumega (100 micro g/kg(-1)/d(-1)) were administered s.c. for 14 days beginning one day following the final dose of carboplatin. The results showed that rhIL-11 significantly improved mean platelet nadirs and shortened the mean duration of platelet counts less than 50% of pre-treatment values. Administration of rhIL-11 also resulted in moderate increase of the reticulated platelet, leukocyte and reticulocyte counts in peripheral blood and megakaryocytic and erythroid progenitors in bone marrow. rhIL-11 did not enhance ADP-induced platelet aggregation. These results indicate that rhIL-11 has a potent thrombopoietic effect in vivo and could be an important agent to reduce the severity and duration of thrombocytopenia following chemotherapy.